Clinically, the initial infection by OMV ( taxonomically known as Salmonid herpesvirus 2; SalHV-2 ) appears as a systemic and frequently lethal infection that is associated with oedema and haemorrhages. Virus multiplication in endothelial cells of blood capillaries, haematopoietic tissue and hepatocytes underlies the clinical signs ( 7, 11 ) . Four months after this first clinical condition, a varying number of surviving fish exhibit epithelioma occurring mainly around the mouth ( upper and lower jaw ) and, to a lesser extent, on the caudal fin, operculum and body surface. These neoplasia may persist for up to 1 year post-infection. In the case of coho salmon, 1-year-old infected fish in particular show ulcers on the skin, white spots on the liver and neoplastic tissues around the mouth parts or body surface. In rainbow trout, the diseased fish exhibit almost no external signs, although some fish manifest ulcerative lesions on the skin. Internally, intestinal haemorrhage and white spots on the liver are observed ( 5, 15, 16 ) .

Following the septicaemia phase of OMV infection, an immune response takes place that results in the synthesis of neutralising antibodies to OMV. A carrier state frequently occurs that leads to virus shedding via the sexual products at the time of spawning.

On the basis of antigenic studies conducted with neutralising polyclonal rabbit antisera, OMV differs from Salmonid herpesvirus 1 ( SalHV-1 ) , which is present in the western United States of America and is only weakly pathogenic ( 3, 9, 12 ) .

The reservoirs of OMV are clinically infected fish and covert carriers among groups of cultured, feral or wild fish. Infectious virus is shed via faeces, urine, sexual products and probably skin mucus, while the kidney, spleen, liver and tumours are the sites where virus is the most abundant during the course of overt infection. The transmission of OMV is horizontal and possibly 'egg-surface associated'. Horizontal transmission may be direct or vectorial, water being the major abiotic factor. Animate vectors and inanimate objects also act in OMV transmission. Disinfection of the eggs just after fertilisation and eyed stage is effective in preventing OMV infection. OMV disease was not reported in alevins originating from disinfected eggs that had been incubated and hatched in virus-free water ( 14 ) .

Salmonids are the only fish species susceptible to OMV infection; the order of the fish species from the most to the least susceptible is: kokanee salmon, chum salmon, masou salmon, coho salmon and rainbow trout. The age of the fish is critical and 1-month-old alevins are the most susceptible target for virus infection ( 6 ) . The main environmental factor favouring OMV infection is low water temperature ( below 14°C )( 10 ) .

The screening procedures for OMV are based on direct isolation of the virus in cell culture and co-culture of neoplastic tissues with salmonid cell lines ( 8 ) . Confirmatory testing is by immunological identification using neutralisation or immunofluorescence tests, and virus-specific gene detection using polymerase chain reaction.

Control methods currently rely on the implementation of avoidance and hygiene practices in the operating of salmonid husbandry. The thorough disinfection of fertilised eggs and the incubation of these eggs and rearing of fry and alevins in premises completely separated from those harbouring virus carriers and free from contact with inanimate objects are the key measures needed to decrease contamination of OMV in a defined fish production site ( 14 ) .